Glutathione and Ultrastructural Changes in Inflow Occlusion of Rat Liver

Armeni, Tatiana; Ghiselli, Roberto; Balercia, Giancarlo; Goffi, Luigi; Jassem, Wayel; Saba, Vittorio; Principato, Giovanni

doi:10.1006/jsre.1999.5781

Cited by 18 publications

(15 citation statements)

References 34 publications

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“…DISCUSSION I/R liver injury is a complex, multifactorial pathophysiologic process. It is generally believed that the process of hepatic I/R includes three different events (Armeni et al, 2000): Hepatic ischemia, portal venous congestion, and subsequent hepatic reperfusion with arterial blood and congested portal blood. Previous study mainly focused on the process of hepatic ischemia and subsequent reperfusion with blood.…”

Section: Table 4 Incidence Of Bacterial Translocation In the Differenmentioning

confidence: 99%

Intestinal microflora in rats with ischemia/reperfusion liver injury

Xing

Li²,

Xu³

et al. 2005

J Zheijang Univ Sci B

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Abstract:Objectives: To investigate the intestinal microflora status related to ischemia/reperfusion (I/R) liver injury and explore the possible mechanism. Methods: Specific pathogen free grade Sprague-Dawley rats were randomized into three groups: Control group (n=8), sham group (n=6) and I/R group (n=10). Rats in the control group did not receive any treatment, rats in the I/R group were subjected to 20 min of liver ischemia, and rats in the sham group were only subjected to sham operation. Twenty-two hours later, the rats were sacrificed and liver enzymes and malondialdehyde (MDA), superoxide dismutase (SOD), serum endotoxin, intestinal bacterial counts, intestinal mucosal histology, bacterial translocation to mesenteric lymph nodes, liver, spleen, and kidney were studied. Results: Ischemia/reperfusion increased liver enzymes, MDA, decreased SOD, and was associated with plasma endotoxin elevation in the I/R group campared to those in the sham group. Intestinal Bifidobacteria and Lactobacilli decreased and intestinal Enterobacterium and Enterococcus, bacterial translocation to kidney increased in the I/R group compared to the sham group. Intestinal microvilli were lost, disrupted and the interspace between cells became wider in the I/R group. Conclusion: I/R liver injury may lead to disturbance of intestinal microflora and impairment of intestinal mucosal barrier function, which contributes to endotoxemia and bacterial translocation to kidney.

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Section: Table 4 Incidence Of Bacterial Translocation In the Differenmentioning

confidence: 99%

Intestinal microflora in rats with ischemia/reperfusion liver injury

Xing

Li²,

Xu³

et al. 2005

J Zheijang Univ Sci B

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“…These results were expected but this determination was performed so that we could establish and verify the differences detected when analyzing the biochemistry of hepatic tissue. The activation of Kupffer cells and neutrophils caused by ischemia and reperfusion themselves may be mediated by the platelet activating factor, favoring the release of oxygen-derived free radicals and increased calcium influx especially after reperfusion, and reduction of the antioxidant agents superoxide dismutase, catalase and GSH 6,7,8,11,12 , leading to a reduction in NADPH and limiting the peroxide reduction by the antioxidant GSH system and increasing MDA production. Phospholipase activation may cause severe damage to the membrane lipids, changes in mitochondrial permeability and in DNA, proteins, lipids and other macromolecules and oxidative stress progressed during ischemia and triggered the oxidative injury after reperfusion 6,7,8,10,12,13 .…”

Section: Discussionmentioning

confidence: 99%

“…This system of reduction by GSH is one of the processes used by the mitochondria to remain stable. During ischemic and reperfusion processes there is a loss of the mitochondiral antioxidant ability and the cells become more sensitive to the effects of excessive production of oxygenderived free radicals, and these changes are detected by the appearance of lipoperoxidation products such as MDA and the decrease in hepatic mitochondrial GSH content 6,7,8,9,11,12,13,14 . The occurrence of lipid peroxidation is measured by the increase in hepatic mitochondrial MDA and by the decrease in hepatic mitochondrial GSH that occurs after liver reperfusion 14 .…”

Section: Discussionmentioning

confidence: 99%

“…Glucose 6-phosphate preferentially maintains sufficient blood glucose levels to supply energy to the brain and other tissues, and the glucose that is not immediately utilized is stored as hepatic glycogen. During the process of ischemia/reperfusion, changes occur in these metabolic pathways and the modified energy metabolism may worsen the pre-existing hepatic dysfunction 3,4,5,6,7,8 . Previous studies from our laboratory have shown a change in the metabolic pattern of the liver from the glycogenetic to glycolytic way due to a functional ischemic process during extrahepatic biliary obstruction (A).…”

Section: Introductionmentioning

confidence: 99%

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Pyruvate kinase activation and lipoperoxidation after selective hepatic ischemia in Wistar rats

et al. 2006

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Purpose: Hepatic ischemia and reperfusion can cause several problems in hepatic surgery. The aim of this study was to determine pyruvate kinase activation and lipid peroxidation after hepatic ischemia. Methods: Twenty-four Wistar rats were submitted to 90 minutes of selective liver ischemia and 15 minutes of reperfusion. Twelve animals were submitted to selective liver ischemia and reperfusion (Group A) and the other 12 were submitted to sham operation (Group B). After 15 minutes of reperfusion, the following parameters were measured: mean arterial pressure (MAP), alanine aminotransferase (ALT), glycemia (GLY), hepatic glycogen (GH), pyruvate kinase (PK) activation, hepatic glutathione (GSH) and malondialdehyde (MDA). Analysis of the results were made by the Student t-test and has been considered significant difference for p<0.05. Results: A and B were differents for all parameters analized. Conclusion: The animals of group A showed reperfusion syndrome with a fall in MAP, activation of glycid metabolism through the glycolitic pathway and presence of lipid peroxidation compared to group B. Key words: Pyruvate kinase. Lipid Peroxidation. Liver Ischemia. RESUMO Objetivo:A isquemia e reperfusão hepática podem causar graves repercussões hepatocelulares em cirurgias hepáticas. O objetivo deste estudo foi determinar o comportamento da piruvato EM PORTUGUÊS quinase e a lipoperoxidação após isquemia hepática. Métodos: Foram utilizados vinte e quatro ratos Wistar machos divididos em dois grupos. Doze animais foram submetidos a 90 minutos de isquemia hepática seletiva e reperfusão hepática de por 15 minutos (pressão arterial média (PAM), alanina aminotransferase (ALT), glicemia (GLI), gicogênio hepático (GH), ativação da piruvato quinase (PQ), glutationa hepática (GSH) e malondialdeído (MDA). Os resultados foram analisados utilizando o teste t de Student sendo as diferenças consideradas significativas para p<0,05. Resultados: Verificou-se diferença significativa entre os grupos em todos os parâmetros analisados. Conclusão: Verificou-se que os animais do grupo A mostraram síndrome de reperfusão com queda da PAM, ativação do metabolismo da glicose através da via glicolítica e presença de lipoperoxidação quando comparada com o grupo B. Descritores: Piruvato quinase. Peroxidação Lipídica. Fígado. Isquemia. Reperfusão.

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“…Recently, glutamine has been demonstrated to protect against ischemia/reperfusion (I/R) injury of the gut, heart, liver and skeletal muscle 14 . The mechanism is still incompletely understood and may be partly related to the preservation of GSH content 15,16 . Another study has demonstrated that GLN preconditioning protects effectively against hepatic ischemiareperfusion injury 17 .…”

mentioning

confidence: 99%

Preconditioning with L-alanyl-L-glutamine in a Mongolian Gerbil model of acute cerebral ischemia/reperfusion injury

Pires¹,

Souza

Guimarães³

et al. 2011

Acta Cir. Bras.

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PURPOSE:To investigate the effect of L-alanyl-L-glutamine (L-Ala-Gln) preconditioning in an acute cerebral ischemia/reperfusion (I/R) model in gerbils. METHODS: Thirty-six Mongolian gerbils (Meriones unguiculatus), (60-100g), were randomized in 2 groups (n=18) and preconditioned with saline 2.0 ml (Group-S) or 0.75g/Kg of L-Ala-Gln, (Group-G) administered into the femoral vein 30 minutes prior to I/R. Each group was divided into three subgroups (n=6). Anesthetized animals (urethane, 1.5g/Kg, i.p.) were submitted to bilateral occlusion of common carotid arteries during 15 minutes. Samples (brain tissue and arterial blood) were collected at the end of ischemia (T 0 ) and after 30 (T 30 ) and 60 minutes (T 60 ) for glucose, lactate, myeloperoxidase (MPO), thiobarbituric acid reactive substances (TBARS), glutathione (GSH) assays and histopathological evaluation. RESULTS: Glucose and lactate levels were not different in studied groups. However glycemia increased significantly in saline groups at the end of the reperfusion period. TBARS levels were significantly different, comparing treated (Group-G) and control group after 30 minutes of reperfusion (p<0.05) in cerebral tissue. Pretreatment with L-Ala-Gln promoted a significant increase in cerebral GSH contents in Group-G at T30 (p<0.001) time-point compared with Group-S. At T 30 and T 60 , increased levels of GSH occurred in both time-points. There were no group differences regarding MPO levels. Pyknosis, presence of red neurons and intracellular edema were significantly smaller in Group-G. CONCLUSION: Preconditioning with L-Ala-Gln in gerbils submitted to cerebral ischemia/reperfusion reduces oxidative stress and degeneration of the nucleus (pyknosis) and cell death (red neurons) in the cerebral tissue.

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Glutathione and Ultrastructural Changes in Inflow Occlusion of Rat Liver

Cited by 18 publications

References 34 publications

Intestinal microflora in rats with ischemia/reperfusion liver injury

Intestinal microflora in rats with ischemia/reperfusion liver injury

Pyruvate kinase activation and lipoperoxidation after selective hepatic ischemia in Wistar rats

Preconditioning with L-alanyl-L-glutamine in a Mongolian Gerbil model of acute cerebral ischemia/reperfusion injury

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